Dysfunctional reward processing is a symptom common of major neuropsychiatric disorders including addiction, schizophrenia and depression. Perturbations in neuronal dopamine signaling have been implicated in the etiology of this symptom and is a target of current pharmacotherapies. Less is known about how neuropsychiatric symptoms manifest downstream of altered dopamine signaling, or the mechanisms by which dopamine signaling becomes perturbed in the first place. The ventral pallidum (VP) is a prime suspect that is receiving increasing attention. The VP is the major output of nucleus accumbens (NAc) and a key input back to the ventral tegmental area (VTA). Activity in VP is sensitive to hedonic stimuli and can potently drive motivated behaviors. Yet the VP is heterogeneous containing neurons with diverse neurotransmitters and projection targets. For example, VP glutamate and GABA neurons share similar projection patterns but drive opposite patterns of behavior on reinforcement tasks. Optogenetic activation of NAc D1-type and D2-type medium spiny neurons can similarly bi-directionally influence reinforcement, but how defined NAc and defined VP cell types are connected is unknown. In Aim 1 we employ optogenetic-assisted electrophysiology and reporter mice to establish the cell-type-specific connectivity between NAc and VP. Aim 2 will use in vivo calcium imaging to assess the intrinsic activity of defined VP populations in response to positive and negative valence stimuli and associated contexts. These studies will build on our recent work, address key knowledge gaps, and facilitate a programmatic assessment of the role of VP circuit heterogeneity in reward processing and neuropsychiatric illness.